ArticleScientific reports2019
A gene expression signature in developing Purkinje cells predicts autism and intellectual disability co-morbidity status.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Loss of YY1 in Purkinje cells triggers cerebellar ataxia via Wnt10b-mediated impairment of dendrite development.iScience · 2026Article
- TUBA8 promotes neuronal dendrite development through its 40th alanine.Journal of molecular cell biology · 2026Article
- Article
- New Perspectives on Non-Invasive Cerebellar Stimulation for Social and Affective Functions in Children and Adolescents.Cerebellum (London, England) · 2025Review
- Cerebellar Functions Beyond Movement and Learning.Annual review of neuroscience · 2024Review
- Review
- Cerebellum and neurodevelopmental disorders: RORα is a unifying force.Frontiers in cellular neuroscience · 2023Article
- Ionic Channels as Potential Targets for the Treatment of Autism Spectrum Disorder: A Review.Current neuropharmacology · 2022Review
- Transcriptomic analysis of isolated and pooled human postmortem cerebellar Purkinje cells in autism spectrum disorders.Frontiers in genetics · 2022Article
- Abnormal Cerebellar Development in Autism Spectrum Disorders.Developmental neuroscience · 2021Review
- Pianp deficiency links GABAMolecular psychiatry · 2020Article
- Purkinje cell number-correlated cerebrocerebellar circuit anomaly in the valproate model of autism.Scientific reports · 2019Article
- Intellectual disability and autism spectrum disorders 'on the fly': insights fromDisease models & mechanisms · 2019Review
- Functional Outcomes of Cerebellar Malformations.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Autism spectrum disorder (ASD) is a complex neurodevelopmental disease whose underpinning molecular mechanisms and neural substrates are subject to intense scrutiny. Interestingly, the cerebellum has emerged as one of the key brain regions affected in ASD. However, the genetic and molecular mechanisms that link the cerebellum to ASD, particularly during development, remain poorly understood. To gain insight into the genetic and molecular mechanisms that might link the cerebellum to ASD, we analysed the transcriptome dynamics of a developing cell population highly enriched for Purkinje cells of the mouse cerebellum across multiple timepoints. We identified a single cluster of genes whose expression is positively correlated with development and which is enriched for genes associated with ASD. This ASD-associated gene cluster was specific to developing Purkinje cells and not detected in the mouse neocortex during the same developmental period, in which we identified a distinct temporally regulated ASD gene module. Furthermore, the composition of ASD risk genes within the two distinct clusters was significantly different in their association with intellectual disability (ID), consistent with the existence of genetically and spatiotemporally distinct endophenotypes of ASD. Together, our findings define a specific cluster of ASD genes that is enriched in developing PCs and predicts co-morbidity status.
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Registered trials
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